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Head Trauma

  • Author: Craig R Ainsworth, MD; Chief Editor: John Geibel, MD, DSc, MSc, MA  more...
 
Updated: Jan 09, 2015
 

Background

Traumatic brain injury (TBI) continues to be an enormous public health problem, even with modern medicine in the 21st century. Most patients with TBI (75-80%) have mild head injuries; the remaining injuries are divided equally between moderate and severe categories.

The cost to society of TBI is staggering, from both an economic and an emotional standpoint. Almost 100% of persons with severe head injury and as many as two thirds of those with moderate head injury will be permanently disabled in some fashion and will not return to their premorbid level of function. In the United States, the direct cost of care for patients with TBI, excluding inpatient care, is estimated at more than $25 billion annually. The impact is even greater when one considers that most severe head injuries occur in adolescents and young adults.

For excellent patient education resources, visit eMedicineHealth's First Aid and Injuries Center and Eye and Vision Center. Also, see eMedicineHealth's patient education articles Concussion, Bicycle and Motorcycle Helmets, and Black Eye.

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Epidemiology

Frequency

The annual incidence of TBI in the United States has been estimated to be 180-220 cases per 100,000 population. In the United States, with a population of almost 300 million, approximately 600,000 new TBIs occur per year. As many as 10% of these injuries are fatal, resulting in almost 550,000 persons hospitalized annually in the United States with head injuries.

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Etiology

While various mechanisms may cause TBI, the most common causes include motor vehicle accidents (eg, collisions between vehicles, pedestrians struck by motor vehicles, bicycle accidents), falls, assaults, sports-related injuries, and penetrating trauma.

Motor vehicle accidents account for almost half of the TBIs in the United States, and in suburban/rural settings, they account for most TBIs. In cities with populations greater than 100,000, assaults, falls, and penetrating trauma are more common etiologies of head injury.

The male-to-female ratio for TBI is nearly 2:1, and TBI is much more common in persons younger than 35 years.

Motorcycle-related head injury

Motorcycle-related head injuries deserve special mention. Motorcycle rights organizations dedicated to promoting safety and to preserving individual freedom suggest that safety should be a choice rather than a requirement; safety is a good choice, but individual motorcyclists should have the right to make a bad choice that ends in disaster if they so choose. A hallmark of the antihelmet movement is the argument that motorcyclists who do not wear helmets can perceive (ie, see and hear) their environment more effectively and, thus, can avoid impending accidents by anticipating them earlier. This argument is fallacious.

Most accidents involving adult, otherwise responsible, motorcyclists are caused by moving objects hitting motorcyclists or by motorcyclists hitting a stationary object after being forced into an unusual position in an attempt to avoid something in their path. A full-face helmet restricts a relatively small portion of inconsequential downward and lateral peripheral vision. Similarly, it is highly improbable that a motorcyclist will hear an impending accident. A marginal increase in the ability to hear road noise and to see downward and laterally is not an improvement in the ability to avoid most accidents.

The medical literature regarding motorcyclists’ head injury is clear. Head trauma is a devastating injury for motorcyclists and their families, and rehabilitation for survivors is prolonged and expensive. Injury expenses for motorcyclists who do not wear helmets far exceed that of motorcyclists who wear helmets. More importantly, the burden of caring for a motorcyclist with a head injury is frequently borne by the taxpayers, regardless of the insurance status of the injured motorcyclist.

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Pathophysiology

Appropriate management of TBI requires an understanding of the pathophysiology of head injury. In addition to the obvious functional differences, the brain has several features that distinguish it from other organ systems. The most important of these differences is that the brain is contained within the skull, a rigid and inelastic container. Because the brain is housed within this inelastic container, only small increases in volume within the intracranial compartment can be tolerated before pressure within the compartment rises dramatically. This concept is defined by the Monro-Kellie doctrine, which states that the total intracranial volume is fixed because of the inelastic nature of the skull. The intracranial volume (V i/c) is equal to the sum of its components, as follows:

V i/c = V (brain) + V (cerebrospinal fluid) + V (blood)

In the typical adult, the intracranial volume is approximately 1500 mL, of which the brain accounts for 85-90%, intravascular cerebral blood volume accounts for 10%, and cerebrospinal fluid (CSF) accounts for the remainder (< 3%). When a significant head injury occurs, cerebral edema often develops, which increases the relative volume of the brain. Because the intracranial volume is fixed, the pressure within this compartment rises unless some compensatory action occurs, such as a decrease in the volume of one of the other intracranial components. This is intimately related to the concept of intracranial compliance, which is defined as the change in pressure due to changes in volume.

Compliance = Change in volume / change in pressure

Compliance is based on the pressure volume index (PVI) within the intracranial compartment. The PVI describes the change in intracranial pressure (ICP) that occurs when a small amount of fluid is added to or withdrawn from the intracranial compartment. Simply stated, the brain has very limited compliance and cannot tolerate significant increases in volume that can result from diffuse cerebral edema or from significant mass lesions, such as a hematoma. The rationale for each treatment of head injury is based on the concept of the Monro-Kellie doctrine and how a particular intervention affects the intracranial compliance. When the volume of any of the components of the total intracranial volume is decreased, the ICP may be decreased.

A second crucial concept in TBI pathophysiology is the concept of cerebral perfusion pressure (CPP). CPP is defined as the difference between the mean arterial pressure (MAP) and the ICP.

CPP = MAP - ICP

In practical terms, CPP is the net pressure of blood delivery to the brain. In the noninjured brain in individuals without long-standing hypertension, cerebral blood flow (CBF) is constant in the range of MAPs of 50-150 mm Hg. This is due to autoregulation by the arterioles, which will constrict or dilate within a specific range of blood pressure to maintain a constant amount of blood flow to the brain.

When the MAP is less than 50 mm Hg or greater than 150 mm Hg, the arterioles are unable to autoregulate and blood flow becomes entirely dependent on the blood pressure, a situation defined as pressure-passive flow. The CBF is no longer constant but is dependent on and proportional to the CPP. Thus, when the MAP falls below 50 mm Hg, the brain is at risk of ischemia due to insufficient blood flow, while a MAP greater than 160 mm Hg causes excess CBF that may result in increased ICP. While autoregulation works well in the noninjured brain, it is impaired in the injured brain. As a result, pressure-passive flow occurs within and around injured areas and, perhaps, globally in the injured brain.

TBI may be divided into 2 categories, primary brain injury and secondary brain injury. Primary brain injury is defined as the initial injury to the brain as a direct result of the trauma. This is the initial structural injury caused by the impact on the brain, and, like other forms of neural injury, patients recover poorly. Secondary brain injury is defined as any subsequent injury to the brain after the initial insult. Secondary brain injury can result from systemic hypotension, hypoxia, elevated ICP, or as the biochemical result of a series of physiologic changes initiated by the original trauma. The treatment of head injury is directed at either preventing or minimizing secondary brain injury.

Elevated ICP may result from the initial brain trauma or from secondary injury to the brain. In adults, normal ICP is considered 0-15 mm Hg. In young children, the upper limit of normal ICP is lower, and this limit may be considered 10 mm Hg. Elevations in ICP are deleterious because they can result in decreased CPP and decreased CBF, which, if severe enough, may result in cerebral ischemia. Severe elevations of ICP are dangerous because, in addition to creating a significant risk for ischemia, uncontrolled ICP may cause herniation. Herniation involves the movement of the brain across fixed dural structures, resulting in irreversible and often fatal cerebral injury.

Maloney-Wilensky et al found that in patients with TBI, brain hypoxia as measured by brain tissue oxygen levels is associated with worse outcome.[1] Their review showed that, in 150 patients with severe TBI, those with brain tissue oxygen levels below 10 mm Hg had worse outcomes (odds ratio [OR], 4.0) and higher mortality (OR, 4.6). However, use of direct brain tissue oxygen probes proved to be safe, with only 2 adverse events in 292 patients.[1] The researchers suggest that treatment to increase brain tissue oxygen levels deserves investigation as a possible means of improving outcome in severe TBI.

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Presentation

TBI may be divided into 2 broad categories, closed head injury and penetrating head injury. This is not purely a mechanistic division because some aspects of the treatment of these 2 types of TBIs differ. The clinical presentation of the patient with TBI varies significantly, from an ambulatory patient complaining of a sports-related head injury to the moribund patient arriving via helicopter following a high-speed motor vehicle accident.

The Glasgow Coma Scale (GCS) developed by Jennett and Teasdale is used to describe the general level of consciousness of patients with TBI and to define broad categories of head injury.[2] The GCS is divided into 3 categories, eye opening (E), motor response (M), and verbal response (V). The score is determined by the sum of the score in each of the 3 categories, with a maximum score of 15 and a minimum score of 3, as follows:

GCS score = E + M + V

Table 1. Glasgow Coma Scale (Open Table in a new window)

Eye Opening
Score 1 Year or Older 0-1 Year
4 Spontaneously Spontaneously
3 To verbal command To shout
2 To pain To pain
1 No response No response
Best Motor Response
Score 1 Year or Older 0-1 Year
6 Obeys command  
5 Localizes pain Localizes pain
4 Flexion withdrawal Flexion withdrawal
3 Flexion abnormal (decorticate) Flexion abnormal (decorticate)
2 Extension (decerebrate) Extension (decerebrate)
1 No response No response
Best Verbal Response
Score >5 Years 2-5 Years 0-2 Years
5 Oriented and converses Appropriate words Cries appropriately
4 Disoriented and converses Inappropriate words Cries
3 Inappropriate words; cries Screams Inappropriate crying/screaming
2 Incomprehensible sounds Grunts Grunts
1 No response No response No response

 

Patients who are intubated are unable to speak, and their verbal score cannot be assessed. They are evaluated only with eye opening and motor scores, and the suffix T is added to their score to indicate intubation. In intubated patients, the maximal GCS score is 10T and the minimum score is 2T. The GCS is often used to help define the severity of TBI. Mild head injuries are generally defined as those associated with a GCS score of 13-15, and moderate head injuries are those associated with a GCS score of 9-12. A GCS score of 8 or less defines a severe head injury. These definitions are not rigid and should be considered as a general guide to the level of injury.

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Indications

Traumatic injury and brain failure

As a type of organ system failure, brain failure invariably affects consciousness. Consciousness is structurally produced in the cerebral hemispheres, including the pons and the medulla. These structures are all interconnected by the reticular formation, which begins in the medulla and extends to the midbrain, where it forms the reticular activating system. This pathway modulates the perception of events and controls integrated responses.

Clinical evaluation of consciousness states is heavily dependent on the findings from the physical examination. When the physical examination yields visual and palpable clues to the integrity of consciousness, impairment thereof may be classified into one of the following categories:

  • Cloudy consciousness: This state is defined as a mild deficit in the speed of information processing by the brain. This results from macrotearing and histological-level disruption of cell-to-cell connectivity occurring throughout the brain disrupting physical connectivity between brain regions, exacerbated by vascular compromise of a mechanical and/or biochemical nature causing islands of nonfunctional or impaired tissue in the brain parenchyma. Cloudy consciousness may be noted after mild-to-moderate head trauma and may persist for several months. Memory of recent events is often diminished, but long-term memory typically remains intact.
  • Lethargy: This state is defined as a decrease in alertness, resulting in impaired ability to perform tasks that are normally accomplished without effort. Patients rouse briefly in response to stimuli and then settle back into inactivity when left alone. They retain awareness of their immediate environment.
  • Obtundation: This state is defined as a decrease in awareness and alertness, in which patients rouse briefly in response to stimuli and follow simple commands but are unaware of their immediate surroundings. When stimulation ceases, they settle back into inactivity.
  • Stupor: In this state, patients cannot communicate clearly but can be aroused by continued painful stimulation. Arousal may be manifested only as withdrawal from painful stimuli. As soon as stimuli are removed, the patient settles back into inactivity.
  • Coma: In this state, patients do not respond to even the most vigorous stimuli.
  • Brain death: This state is equivalent to functional decapitation and is characterized by irreversible cessation of whole-brain function and hemisphere and brainstem function.

The efficacy of the physical examination in the evaluation of consciousness diminishes when visual clues disappear (eg, during heavy sedation, therapeutic musculoskeletal paralysis). In such situations, monitoring of cerebral function by compressed spectral array is helpful in assessing the effect of therapy on neuronal function.

Processed electroencephalogram (compressed spectral array) in consciousness assessment

The processed electroencephalogram (EEG) does not require as many head electrodes to generate a satisfactory signal that can be used for clinical data in the intensive care unit (ICU). Brain wave monitoring by portable, noninvasive computer processed monitors allow quick recognition of some brain functions under titrated suspended animation in real time. These parameters are not effectively evaluated by raw signal EEG monitors, but some progress has been made using computerized processed signal EEGs. Advantages of the processed EEG during neuromuscular blockade are that data are more easily interpreted by clinicians not specifically trained in electroencephalography.

The continuum from wakefulness to sleep involves a progressive decrease in the alpha band followed by increased activity in the beta, theta, and delta bands. The alpha rhythm contains waves of 8-12 Hz and is very responsive to volitional mental activity, increasing with excitement and decreasing with tranquility. These rhythms occur mainly in the posterior head and are the predominant brain activity in the normal brain.

A technique has been developed to simplify pattern recognition and interpretation of the brain electrical activity using the key word SAFE:

  • S - SYMMETRY - Compare the pattern of asymmetrical patterns. Can indicate diminished perfusion to one hemisphere, cerebral embolism, or thrombosis.
  • A - AMPLITUDE - Compare the altitude of the vectors. Asymmetric hemispherical amplitude suggests agitation under paralysis. Low amplitude suggests sedation and quiescence.
  • F - FREQUENCY - Compare the distribution of vectors throughout all frequency bands. Absent or attenuated activity in the “conscious” side suggests sedation or anesthesia.
  • E - EDGE - Observe the activity edge. Significant dips in one hemisphere compared to the other suggest focal brain ischemia.

Agitation is represented by linear activity depicting intensity of brain activity and position of this activity within the brain topography. Sedation can be effectively titrated until this activity is reduced to normalcy using continuous infusion of sedative agents, while ensuring patient comfort under paralysis as the search for underlying pathology follows. Different classifications and combinations of sedatives, analgesics, or antipsychotics can be tried until the combination that brings about the most appropriately calm cerebral function tracing is discovered. Attention can then be turned to protecting other organs from damage.

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Relevant Anatomy

Several aspects of neuroanatomy and neurophysiology require review in a discussion of TBI. Although a comprehensive review of neuroanatomy is beyond the scope of this discussion, a few key concepts are reviewed.

The brain essentially floats within the CSF; as a result, the brain can undergo significant translation and deformation when the head is subjected to significant forces. In a deceleration injury, in which the head impacts a stationary object, such as the windshield of a car, the skull stops moving almost instantly. However, the brain continues to move within the skull toward the direction of the impact for a very brief period after the head has stopped moving. This results in significant forces acting on the brain as it undergoes both translation and deformation.

In an acceleration injury, as in a direct blow to the head, the force applied to the skull causes the skull to move away from the applied force. The brain does not move with the skull, and the skull impacts the brain, causing translation and deformation of the brain. The forces that result from either deceleration or acceleration of the brain can cause injury by direct mechanical effects on the various cellular components of the brain or by shear-type forces on axons. In addition to the translational forces, the brain can experience significant rotational forces, which can also lead to shear injuries.

The intracranial compartment is divided into 3 compartments by 2 major dural structures, the falx cerebri and the tentorium cerebelli. The tentorium cerebelli divides the posterior fossa or infratentorial compartment (the cerebellum and the brainstem) from the supratentorial compartment (cerebral hemispheres). The falx cerebri divides the supratentorial compartment into 2 halves and separates the left and right hemispheres of the brain. Both the falx and the tentorium have central openings and prominent edges at the borders of each of these openings. When a significant increase in ICP occurs, caused by either a large mass lesion or significant cerebral edema, the brain can slide through these openings within the falx or the tentorium, a phenomenon known as herniation. As the brain slides over the free dural edges of the tentorium or the falx, it is frequently injured by the dural edge.

Several types of herniation exist, as follows: (1) transtentorial herniation, (2) subfalcine herniation, (3) central herniation, (4) upward herniation, and (5) tonsillar herniation.

Transtentorial herniation occurs when the medial aspect of the temporal lobe (uncus) migrates across the free edge of the tentorium. This causes pressure on the third cranial nerve, interrupting parasympathetic input to the eye and resulting in a dilated pupil. This unilateral dilated pupil is the classic sign of transtentorial herniation and usually (80%) occurs ipsilateral to the side of the transtentorial herniation. In addition to pressure on the third cranial nerve, transtentorial herniation compresses the brainstem.

Subfalcine herniation occurs when the cingulate gyrus on the medial aspect of the frontal lobe is displaced across the midline under the free edge of the falx. This may compromise the blood flow through the anterior cerebral artery complexes, which are located on the medial side of each frontal lobe. Subfalcine herniation does not cause the same brainstem effects as those caused by transtentorial herniation.

Central herniation occurs when a diffuse increase in ICP occurs and each of the cerebral hemispheres is displaced through the tentorium, resulting in significant pressure on the upper brainstem.

Upward, or cerebellar, herniation occurs when either a large mass or an increased pressure in the posterior fossa is present and the cerebellum is displaced in an upward direction through the tentorial opening. This also causes significant upper brainstem compression.

Tonsillar herniation occurs when increased pressure develops in the posterior fossa. In this form of herniation, the cerebellar tonsils are displaced in a downward direction through the foramen magnum, causing compression on the lower brainstem and upper cervical spinal cord as they pass through the foramen magnum.

Another aspect of the intracranial anatomy that has a significant role in TBI is the irregular surface of the skull underlying the frontal and temporal lobes. These surfaces contain numerous ridges that can cause injury to the inferior aspect of the frontal lobes and the temporal lobes as the brain glides over these irregular ridges following impact. Typically, these ridges cause cerebral contusions. The roof of the orbit has many ridges, and, as a result, the inferior frontal lobe is one of the most common sites of traumatic cerebral contusions.

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Contributor Information and Disclosures
Author

Craig R Ainsworth, MD Medical Director, Intensive Care Unit, Associate Program Director, Internal Medicine Residency Program, Critical Care Medicine Physician, William Beaumont Army Medical Center

Craig R Ainsworth, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Gregory S Brown, Jr, MD Staff Physician, Department of Pulmonary and Critical Care, William Beaumont Army Medical Center

Gregory S Brown, Jr, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians, American College of Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

John Geibel, MD, DSc, MSc, MA Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director, Surgical Research, Department of Surgery, Yale-New Haven Hospital; American Gastroenterological Association Fellow

John Geibel, MD, DSc, MSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, Society for Surgery of the Alimentary Tract

Disclosure: Received royalty from AMGEN for consulting; Received ownership interest from Ardelyx for consulting.

Acknowledgements

David W Crippen, MD, FCCM Associate Professor, Department of Critical Care Medicine, University of Pittsburgh Medical Center; Medical Director, Neurovascular Critical Care, Presbyterian-University Hospital

David W Crippen, MD, FCCM is a member of the following medical societies: American College of Critical Care Medicine, European Society of Intensive Care Medicine, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Michael A Grosso, MD Consulting Staff, Department of Cardiothoracic Surgery, St Francis Hospital

Michael A Grosso, MD is a member of the following medical societies: American College of Surgeons, Society of Thoracic Surgeons, and Society of University Surgeons

Disclosure: Nothing to disclose.

Scott Shepard, MD Assistant Professor, Department of Surgery, Section of Neurosurgery, UMDNJ-Robert Wood Johnson School of Medicine

Disclosure: Nothing to disclose.

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Table 1. Glasgow Coma Scale
Eye Opening
Score 1 Year or Older 0-1 Year
4 Spontaneously Spontaneously
3 To verbal command To shout
2 To pain To pain
1 No response No response
Best Motor Response
Score 1 Year or Older 0-1 Year
6 Obeys command  
5 Localizes pain Localizes pain
4 Flexion withdrawal Flexion withdrawal
3 Flexion abnormal (decorticate) Flexion abnormal (decorticate)
2 Extension (decerebrate) Extension (decerebrate)
1 No response No response
Best Verbal Response
Score >5 Years 2-5 Years 0-2 Years
5 Oriented and converses Appropriate words Cries appropriately
4 Disoriented and converses Inappropriate words Cries
3 Inappropriate words; cries Screams Inappropriate crying/screaming
2 Incomprehensible sounds Grunts Grunts
1 No response No response No response
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